tubular cells of hyperoxaluric rats

In this study, we investigated the protective effect of losartan as an AT1 receptor antagonist by evaluating the expression of apoptosis-regulatory genes that contribute to the progressive damage in the renal tubules of hyperoxaluric rats. Rats were divided into 4 groups of 10 each; control (C), ethylene glycol (EG), ethylene glycol + losartan (EG + L) and Losartan (L). For 4 weeks 0.8% EG, as a precursor for oxalate, was administered to EG and EG + L and losartan (300 mg/l) was administered to groups EG + L and L. Urine and blood samples were collected for biochemical determination. Bcl-2, bax, caspase-3 and TGF-beta 1 antibodies were used for immunohistochemistry. Apoptosis was determined by TUNEL method. A marked increase in urinary oxalate levels of the rats in EG and EG + L groups was found. In the EG group a diffuse amount of oxalate crystals into the tubular lumina and interstitium in the cortex was observed. In the EG group GBM thickening, interstitial fibrosis and tubular atrophy with infiltration of mononuclear cell findings reduced in the EG + L group were presented as well. In the EG group, immunoreactivity of TGF-beta 1 was increased in glomeruli and tubuli. In the EG + L group, immunoreactivity of TGF-beta 1 was decreased compared to the EG group. Bax expression increased in the renal tubules of EG group and reduced in the EG + L group comparing to the control. In the EG + L group, the immunoreactivity of bcl-2 was increased in glomeruli. In EG + L treated group, number of caspase-3 immunopositive cells were decreased compared to all groups (P < 0.01). Apoptotic cells were increased in the EG-treated group compared to the other groups. Decreased apoptotic cell number was observed in the EG + L compared to the EG group (P < 0.01). Our findings suggest that losartan may provide a beneficial effect against tubulointerstitial damage and decrease renal tubular apoptosis caused by hyperoxaluria

SIRT6 expression and oxidative DNA damage in individuals with prediabetes and type 2 diabetes mellitus

Sirtuins (SIRTs) is a family of NAD+ dependent histone deacetylases. SIRT6 takes play in glucose homeostasis, genomic stability and DNA repair. Although increased oxidative DNA damage and decreased DNA repair activity were determined in diabetes mellitus, the possible relation between level of oxidative DNA damage and SIRT6 expression has not been investigated so far. We determined SIRT6 expression and urinary 8-hydroxy deoxyguanosine (8-OHdG) levels, marker of oxidative DNA damage, in cases with prediabetes (PreDM) and type 2 diabetes mellitus (T2DM)

Predicting VO(2)max From Submaximal Exercise and Non-Exercise Data Using Artificial Neural Networks

21st Signal Processing and Communications Applications Conference (SIU) -- APR 24-26, 2013 -- CYPRUSWOS: 000325005300246The purpose of this study is to develop new multilayer feed-forward artificial neural network (ANN)-based maximal oxygen uptake (VO(2)max) prediction models by using submaximal treadmill exercise and nonexercise data. Using 10-fold cross validation on the dataset, standard error of estimate (SEE) and multiple correlation coefficient (R) of the models are calculated. It is shown that the models including submaximal, standard nonexercise and questionnaire variables yield higher R and lower SEE than the ones including submaximal and standard nonexercise variables only. The results of ANN-based models are also compared with the ones obtained by Multiple Linear Regression (MLR) and Support Vector Machines (SVM). It is shown that ANN-based models perform better than MLR and SVM-based models for predicting VO(2)max

The neuroprotective effects of z-DEVD.fmk, a caspase-3 inhibitor, on traumatic spinal cord injury in rats

Background: Apoptosis is one of the most important forms of cell death seen in a variety of physiological and pathological conditions, including traumatic injuries. This type of cell death occurs via mediators known as caspases. Previous studies have investigated the roles that apoptosis and different caspases play in the pathogenesis of secondary damage after spinal cord injury (SCI). The aim of this research was to assess the neuroprotective effect of z-DEVD.frnk, a caspase-3 inhibitor, in a rat model of SCI